PAG1 knockdown in NB cells promotes proliferation and anchorage-independent colony formation with increased activation of AKT and ERK downstream of c-Src, while PAG1 overexpression significantly rescues these effects.
AKT (v-akt murine thymoma viral oncogene homolog 1) and N-Ras (neuroblastoma ras viral oncogene homolog) coactivation in the mouse liver promotes rapid carcinogenesis by way of mTOR (mammalian target of rapamycin complex 1), FOXM1 (forkhead box M1)/SKP2, and c-Myc pathways.
We have previously demonstrated an increased expression of gastrin-releasing peptide (GRP) and its receptor, GRPR, in neuroblastoma and that GRP activates the PI3K-AKT pathway as a proangiogenic factor during tumor progression.
Our previous report revealed that <i>Drynaria fortunei</i> (Polydiaceae) protected against 6-hydroxydopamine (6-OHDA)-induced oxidative damage via the PI3K/AKT pathway in B35 neuroblastoma cells.
In this study, we measured the expression level of GIGYF1, Grb10, phosphorylated IGF1R/IGF1R, phosphorylated AKT serine/threonine protein kinase/protein kinase B (AKT)/AKT, and phosphorylated extracellular signal-regulated kinase (ERK)/ERK in human neuroblastoma SHSY-5Y cells.
Proximity ligation and two-way immunoprecipitation assays using monoclonal antibodies against gB and Akt-1 phosphorylated at S473 [Akt-1(S473)] confirmed that HSV-1(McKrae) gB interacted with Akt-1(S473) during virus entry into human neuroblastoma (SK-N-SH) cells and induced the release of intracellular calcium.
Here we report that membrane depolarization triggered IKC intracellular signals mediated by small GTPases of the Ras subfamily and protein kinase B (Akt) to advance the development of filopodia and lamellipodia in Chinese hamster ovary cells, stimulate their motility, and enhance neurite outgrowth in mouse neuroblastoma Neuro2a cells.
This growth effect was accompanied by a marked decrease in the expression of MYC, MYCN, AKT and an increase in p53 expression in neuroblastoma cell lines without TP53 mutation.
These results suggest that repression of Survivin by FKHRL1 facilitates FKHRL1-induced apoptosis and sensitizes to cell death induced by DNA-damaging agents, which supports the central role of PI3K-PKB-FKHRL1 signaling in drug resistance of human NB.
The present study was aimed to explore the neuroprotective effect of AA against aluminium maltolate <b>(</b>Al(mal)<sub>3</sub>) induced neurotoxicity by assessing cell viability, mitochondrial membrane potential, levels of reactive oxygen species (ROS), DNA damage and apoptosis (Hoechst and dual staining, comet assay; expressions of pro-apoptotic, anti-apoptotic and signaling indices) via AKT/GSK-3β signaling pathway in SH-SY 5Y neuroblastoma cells.
The detected variants are located within the different domains of TIAM1 that signal to the upstream regulator RAS and downstream effector molecules MYC and RAC, which are all implicated in neuroblastoma etiology and progression.
BCH motif-containing molecule at the carboxyl terminal region 1 (BMCC1)/PRUNE2 is highly expressed in patients with favorable neuroblastoma (NB), encoding a multifunctional scaffold protein that modulates several signaling networks including RhoA and AKT pathways.
In summary, we found NLGN3 promoted neuroblastoma cell proliferation and growth through activating PI3K/AKT pathway and providing a new target for neuroblastoma therapy.
In contrast to RAS-MAPK pathway-mutated neuroblastoma cell lines, ALK-addicted neuroblastoma cells treated with trametinib showed increased activation (inferred by phosphorylation) of the kinases AKT and ERK5.
We then demonstrate that the uptake of NB exosomes by MSCs was associated with a rapid increase in ERK1/2 and AKT activation, and that blocking ERK1/2 but not AKT activation inhibited the IL-6 and IL-8/CXCL8 production by MSCs without affecting exosome uptake.
In this study we investigated the phosphorylation status of key proteins in the PI3K/AKT/mTOR pathway and the effects of the mTOR inhibitors rapamycin and CCI-779 on neuroblastoma tumorigenesis.